B cells play a regulatory role in mice infected with the L3 of Brugia pahangi
B cells play a regulatory role in mice infected with the L3 of Brugia pahangi
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DOI：
10.1093/intimm/dxh217
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发表时间：
2005-04-01
影响因子：
4.4
通讯作者：
Devaney, E
中科院分区：
文献类型：
--
作者：
Gillan, V;Lawrence, RA;Devaney, E
感染帕汉布氏丝虫L3的小鼠产生强烈的T(H)2反应，其特征是抗原特异性IL-4、IL-5和IL-10水平升高。在这里，我们表明，这些动物的B细胞是体外主要的增殖群体，B细胞耗尽或感染MU MT小鼠，导致抗原特异性增殖水平降低。B细胞也可以作为抗原提呈细胞(APC)到CD4(+)细胞，这从B细胞耗尽时细胞因子谱的变化中可以看出。IL-10在体外和体内均下调B细胞表面B7-1和B7-2的表达，从而降低B细胞的抗原提呈效率。因此，IL-10可能通过抑制B细胞上B7配体的表达来调节L3感染小鼠的CD4反应。为了支持这一假设，在体内阻断IL-10R会导致CD4(+)细胞的增殖增加。我们认为B细胞参与了一个负反馈循环：由L3感染而产生的IL-10下调了B细胞表面B7分子的表达，减弱了它们作为APC对CD4(+)T细胞的作用，并限制了它们的增殖。
Mice infected with the L3 of the filarial nematode Brugia pahangi make a strong T(h)2 response characterized by elevated levels of antigen-specific IL-4, IL-5 and IL-10. Here we show that B cells from these animals are the major proliferating population in vitro with depletion of B cells or infection of mu MT mice, resulting in reduced levels of antigen-specific proliferation. B cells also act as antigen-presenting cells (APC) to CD4(+) cells as demonstrated by the switch in cytokine profiles upon B cell depletion. The efficiency of B cells in antigen presentation is attenuated by IL-10 which down-regulates the expression of B7-1 and B7-2 on the surface of B cells both in vitro and in vivo. Thus, IL-10 may modulate CD4 responses in L3-infected mice by suppressing the expression of B7 ligands on B cells. In support of this hypothesis, blockade of the IL-10R in vivo results in increased proliferation of CD4(+) cells. We propose that B cells participate in a negative feedback loop: IL-10 elicited by infection with L3 and produced by B cells (and CD4(+) cells) down-regulates the expression of B7 molecules on the B cell surface, attenuating their efficiency as APC to CD4(+) T cells and restricting their expansion.